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“This loss of gray matter is a complement
of the axonal loss and the genesis
of symptomatic progression in MS,” Mr.
Achiron said. “Identification of these
specific areas of loss has clinical relevance
for understanding the associated
cognitive changes.”

And of course, from Cheerleader's wonderful Bologna notes:

Dr. Bianca Weinstock-Guttman, Jacobs Neurological InstituteThe MS patients had a decrease in brian volume, and less gray matter volume than the controls. The third ventricle was dilated compared to controls.

The velocity of the CSF- the average net CSF flow in MS patients was strongly associated with a retrograde flow- velocity is lower in both directions in MS

The more abnormal the criteria, the more the gray matter loss, the more brain atrophy, the worse the disease progression- the more venous stenosis was found.

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Hey Mark-
That's a new paper. Thanks. There are five new papers out on gray matter loss and MS from November 2009- present. More and more researchers are finding the link to gray matter loss and disability and progression. We have often noted on here that it's "NOT about the white matter lesions" since many of our members have few or none, and are progressive. This is why it is ESSENTIAL that patients are tested for venous insufficiency and treated before the brain atrophies..

Dr. Rudick and colleagues at the Cleveland Clinic, who have been following 85 MS patients and healthy controls since 2000, reported in the July 15 Journal of Neurological Science that the gray matter volume in patients decreases over time. Early in the disease, Dr. Rudick said, gray matter volume loss proceeds three times faster in patients than in controls.As the disease progresses — and the symptoms worsen — “the rate of atrophy in patients increases to 14 times that seen in unaffected people,” Dr. Rudick added. “What's more, gray matter atrophy correlates with physical disability and cognitive disability more strongly than white matter atrophy.”As the evidence for this two-hit hypothesis strengthens, scores of laboratories are trying to find imaging tools to identify gray matter pathology and develop therapies that slow or stop the cortical degeneration. The therapies now in development target white matter pathology. And scientists still have to figure out the relationship between the inflammation in the white matter and the cortical damage.

The basal ganglia in haemochromatosisHaemochromatosis is characterised by deposition of ironcontaining
pigment in various organs, but little is known about possible
deposition in the brain and its clinical impact. We therefore investigated
14 patients with hereditary haemochromatosis with MRI,
CT and transcranial ultrasound (TCS) and examined them neurologically.
In six of the patients dense lesions were found within the lentiform
nucleus on CT, all of whom displayed hyperechogenic lesions in
the same area on TCS, as did one other patient. In these patients the
relative signal intensities of the lentiform nucleus measured by MRI
relaxometry were higher. No patient had clinical signs of basal ganglia
disorders.

cheerleader wrote:Hey Mark-That's a new paper. Thanks. There are five new papers out on gray matter loss and MS from November 2009- present. More and more researchers are finding the link to gray matter loss and disability and progression. We have often noted on here that it's "NOT about the white matter lesions" since many of our members have few or none, and are progressive. This is why it is ESSENTIAL that patients are tested for venous insufficiency and treated before the brain atrophies..

Neurologists aren't ignoring gray matter atrophy--that is one of the hottest topics these days. Whether CCSVI treatment serves to alleviate that, however remains to be seen. Neurologists have been fairly up front about the fact that "lesion load does not correlate with disability." --those exact words are bandied around quite a bit. ...just to clarify. I am as hopeful as all of you that CCSVI will indeed halt brain atrophy, but it will realistically take years of observing MS brains to really "prove" that.

dx RRMS Jun. 2009...on Copaxone and LDN and waiting for my turn to be "liberated"<br />

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